The invention relates generally to a method for preventing and/or treating stress-induced gastric injury in persons with a predisposition to such injury.
Gastric discomfort is a common complaint among people. In a healthy human stomach and duodenum, an effective balance exists between the potential for gastric acid and pepsin to damage gastric mucosal cells, and the ability of these cells to protect themselves from injury. Disruption of this balance has been attributed to several factors, including environmental and emotional stress, age, diet, genetics and individual behavior. This disruption is evidenced as a burning, aching or gnawing pain that may be perceived as abdominal pressure or fullness. Most of the symptoms experienced by patients under such conditions result from a breakdown of the normal mucosal defense mechanisms. Various studies have demonstrated that gastric acid and pepsin are important in the pathogenesis of dyspepsia, stomach upset, gastroesophageal reflux disease, and duodenal and gastric ulcer. Several mechanisms are believed to be important in protecting gastric and duodenal mucosa from damage by gastric acid, pepsin, bile pancreatic enzymes, as well as these external stressors/factors. These defense mechanisms include mucus, mucosal blood flow, cell renewal and bicarbonate. These factors acting in balance help maintain mucosal integrity.
Physical stress has been shown to induce significant gastrointestinal mucosal injury in animals. Water-immersion restraint stress of rats results in an increase in cell loss accompanied by an accelerated cell migration and macroscopic mucosal injury. Cell migration was found to be accelerated in fundic mucosa after 90 minutes of exposure to stress. A combination of increased cell loss and depressed epithelial proliferation may play a role in stress-related gastric lesions and injury in the rats. It has been suggested that oxygen free radicals are greatly involved in the pathogenesis of gastric injury. Free radicals may play a major role in stress-induced gastrointestinal injury.
Current treatments for gastric discomfort include administration of antacids and H.sub.2 -receptor antagonists. However, these treatments are not effective in preventing stress-induced gastric injury over the long term. There remains a need for an effective method to prevent and/or treat gastric injury caused by stress in persons who have or are at risk for such injury. The present invention fulfills this need and other needs, and provides further related advantages.